Wednesday, August 26, 2009

This is a 58 year old male with 40 minutes of chest pain of acute onset. He called 911 and paramedics recorded a prehospital 12 lead ECG which showed a clear inferior STEMI (not shown, tracing could not be found). He was given aspirin and sublingual nitroglycerine, which improved his pain. The cath lab was activated by the paramedics. On arrival, the following ECG was recorded.

There is 0.5 mm of ST elevation in inferior leads II, III, and aVF. In addition, the T-waves in II, III, and aVF are very large, significantly larger than normal in both height and width. To diagnose inferior MI, there must always be reciprocal ST depression or T-wave inversion or both in lead aVL (see abstract of our research below). This is present here.

Hyperacute T-waves can be present early, before the ST segment elevates, but they can also be present as ST elevation is resolving from spontaneous reperfusion.

In this case the diagnosis was clear due to the prehospital ECG. But suppose there had been no prehospital ECG? Or if the first ECG had looked like this? Suppose the ST segments were on the way up rather than on the way down. Would you have diagnosed this? This identical ECG could be all the evidence you might have.

If you find yourself in this diagnostic dilemma and you are uncertain of the diagnosis, remember that you can use serial ECGs, old ECGs, and immediate echocardiography to help in the diagnosis.

In acute inferior STEMI, Reciprocal ST depression in aVL and T-wave inversion in aVL are both more sensitive than ST elevation criteria and appear earlier in the course of STEMI

Christine Worrall

Emily Vogel

Stephen W. Smith

Background: A previous study found that reciprocal ST depression (rSTD) is present in only 82% of inferior ST elevation (STE) acute myocardial infarction (MI). However, we believe that changes in lead aVL are far more sensitive. Objectives: To find the incidence of any rSTD or T-wave inversion (TWI) in angiographically proven inferior STEMI. Methods: We searched the catheterization laboratory database for all cases coded as acute Inferior STEMI from January 2002 through March 2008. All cases were reviewed and the presenting ECG, as well as the first ECG that was used for diagnosis of acute STEMI, were analyzed. “True STEMI” was defined as 100% occlusion or as a culprit lesion with maximum troponin I (trop) > 10 ng/ml. STE was measured in leads II, III, aVF; aVL was scrutinized for any rSTD or TWI. TWI was defined as a T-wave mostly down, or a biphasic T-wave that is first down, then up (not up then down, which is associated with lateral AMI). Reperfusion criteria were defined as STE of at least 1 mm in 2 of 3 of inferior leads II, III, aVF. Results: There were 160 unique cases. 107 had 100% occlusion, and 35 had < 100% occlusion, but had a maximum trop > 10 ng/ml, for 142 true STEMI; 18 (11%) had < 100% occlusion and a max trop < 10 ng/ml. 85% of the diagnostic ECGs of true STEMI, and 84% of all cases, met STE criteria. No true STEMI had absence of reciprocal depression in lead aVL. Of the 107 with 100% occlusion, 100 (93%) had at least 0.5 mm of rSTD; the remainder had rSTD of < 0.5 mm. Even among those without true STEMI, 94% had some rSTD in aVL. Additionally, in 44 cases (28%), there was no STE whatsoever on the presenting (first) ECG; all of them had either rSTD or TWI. See Table. Conclusion: STE criteria for inferior STEMI are insensitive, especially on the presenting ECG. Changes in aVL, both some amount of rSTD and also TWI, are more sensitive than STE criteria in the diagnosis of inferior STEMI and are nearly universally present in inferior STEMI. These changes also appear earlier than STE.

This 46 yo male presented with chest pain. There is 1 mm of ST elevation in V1-V3, but there are large QS-waves preceding the STE. Such QS waves are highly suggestive of old transmural MI, with subsequent akinesis or dyskinesis of the anterior wall. Acute MI, if early in its course (first 6 hours, at least), always has tall T-waves in addition to ST elevation.

There is one retrospective study (Smith SW. American Journal of Emergency Medicine 23(3):279-287, May 2005) showing that the T/QRS ratio is significantly greater in acute anterior STEMI than in old anterior MI with persistent ST Elevation. We have since validated this and are writing the manuscript as of November 2014.The best criterion for differentiating was the sum of STE in V1-V4 divided by the sum of the QRS's in V1-V4 (TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4). If this value was greater than 0.22 vs. less than 0.22, then it is likely to be acute STEMI. Another rule that was almost as good: if any one of the leads had a ratio of T to QRS greater than, vs. less than, 0.36, it was very likely to be STEMI.

T-waves in aneurysm may be upright or inverted, but in neither case should they have high voltage. [Deep inversions suggest very recent NSTEMI (e.g., Wellens'). Tall T-waves suggest acute STEMI.]

The above ECG has a summed ratio of 0.05 and is clearly NOT an acute STEMI. It is important to know that only about 70%-80% of patients with the ECG morphology of "LV aneurysm" actually have an LV aneurysm, as defined by echocardiographic dyskinesis. "LV aneurysm" is far less common in this era of reperfusion, in which STEMI is not allowed to progress to full infarction (also known as "transmural" infarction, an old but useful term). The patient above had akinesis and had formerly had a mural thrombus, which is a common complication of an immobile wall which also may have post-infarction inflammation.

This patient ruled out for MI with negative troponins.

Case 2. Exaggeration of persistent STE after old MI by tachycardia

This 65 yo male presented with dyspnea but no CP. The lungs sound wet. The ECG is shown.

There is quite a bit of ST elevation in the anterior leads, but it is preceded by very deep QS waves suggestive of old MI. Previous MI can have persistent ST elevation, and just like in Left Bundle Branch block and other entities, ST elevation may be exaggerated in states of tachycardia. Therefore, the T-wave to QRS ratio may also be exaggerated. Here the formula TV1+TV2+TV3+TV4 divided by QRSV1+QRSV2+QRSV3+QRSV4 = 0.27, substantially greater than 0.22, and would indicate acute STEMI. But one must be suspicous of a false positive in the presence of extreme tachycardia such as this. Also arguing against STEMI is the fact that there is no single T/QRS ratio (V1-V4) greater than 0.36.

The difficult decision is this: is this an old MI with exaggerated persistent STE due to tachycardia, or is it an old MI with a new STEMI superimposed? Given that the BNP was greater than 5000 and the patient had no chest pain, and the high likelihood that such a morphology represented the former (not the latter) diagnosis, the patient was not set up for angiogram and reperfusion.

A previous ECG was found and is shown:

It is evident that there previously was classic LV aneurysm morphology, but with much less ST elevation and shorter T-waves. The ratio here is low.
For rule 1: (4.5 + 7.5 + 4 + 0) divided by (14.5 + 31 + 20 + 19) = 0.19 (less than 0.22)
For rule 2: the lead with the highest ratio is V1: 4.5 divided by 14.5 = 0.31 (less than 0.36)

A previous echo had shown severe decreased LVF with an akinetic anterior wall.

Clinicians correctly interpreted the first ECG as exaggeration of ST elevation of old MI due to tachycardia, stress, and exacerbation of CHF. Treatment of CHF resulted in a slowing heart rate. Follow up confirmed all troponins negative and resolution of ST elevation when the heart rate came down.

This is the prehospital ECG of a 37 year old male with chest pain. It is obviously an acute STEMI, and in this case involved a proximal wraparound LAD supplying the anterior, lateral, and inferior walls. Hence the widespread ST elevation which the computer algorithm interprets as pericarditis. If the computer can make this mistake, you know it can make much less egregious mistakes (and I'll assure you that it does).

Therefore, you must learn to read the ECG yourself.

Comments indicate that I need to explain this better: The ECG represents anterior STEMI, and not pericarditis, because 1) the ST elevation is in right precordial leads (V1-V3) as well as left (V4-V6) [pericarditis has more in the inferior and lateral leads and often looks like an inferolateral STEMI] 2) unlike pericarditis, the T waves are "hyperacute", with straight ST segments; they look wide and bulky 3) there is very poor R wave progression, 4) there is "terminal QRS distortion", meaning the S-wave is obliterated in many leads, particulary V4-V6, and 5) the QT is long. All of these favor acute STEMI over pericarditis.

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Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.